Measles is an acute contagious disease that remains a major cause of childhood mortality worldwide, especially in developing countries (6). Measles virus (MV), a member of the family Paramyxoviridae, is an enveloped virus with a nonsegmented single-stranded negative-sense RNA genome (15). Upon MV infection, cells produce alpha/beta interferon (IFN-␣/␤) following recognition of the virus by RNA helicases encoded by retinoic acid-inducible gene I (RIG-I) and melanoma differentiation-associated gene 5 (MDA5) (22, 43) or Toll-like receptor (TLR) 7 (51). MV encodes phosphoprotein (P) and V and C proteins, which can counteract the host IFN response (11,34,36,54,64). Among these viral proteins, the V protein is the most versatile antagonist. It blocks IFN-␣/␤ signal transduction in infected cells (9,11,13,36,38,47,59,64) and inhibits TLR7-mediated IFN-␣ production in human plasmacytoid dendritic cells (42). Furthermore, the MV V protein, like that of other paramyxoviruses, interacts with MDA5 and inhibits its function with respect to IFN induction (2). The N-terminal domain of the V protein (Vn), which is common to the P and V proteins, has been shown to interact with STAT1 (signal transducer and activator of transcription 1) and Jak1, which are involved in IFN signaling (9), whereas the unique cysteine-rich C-terminal domain of the V protein (Vc) was found to interact with MDA5 (39), STAT2 (47), and IB kinase ␣ (IKK␣), which is involved in the activation of interferon-regulatory factor 7 through TLR7 (42). Furthermore, Vc interacts with the NF-B subunit p65 (RelA) to suppress NF-B activity (53). The mechanism by which the MV C protein acts as an IFN antagonist is not well understood, but it probably suppresses IFN induction by regulating viral RNA synthesis (34).Secretion of the inflammatory cytokines interleukin-1␤ (IL-1␤) and IL-18 is tightly regulated by the inflammasomes known as caspase-1-activating molecular complexes (32). Recognition of pathogens by pattern recognition receptors such as TLRs induces pro-IL-1␤ and pro-IL-18 in the cytoplasm. The activation of the inflammasomes leads to the conversion of procaspase-1 to caspase-1, which cleaves procytokines into mature IL-1␤ and IL-18, which are then secreted. The best-characterized inflammasome is the NOD-like receptor (NLR)-family pyrin domain-containing 3 (NLRP3, also known as Nalp3 or cryopyrin) inflammasome, which can be activated by a wide range of stimuli, such as endogenous danger signals from damaged cells, bacterial components, and environmental irritants (52).Infection by RNA viruses such as influenza virus (1,19,20,61), encephalomyocarditis virus (EMCV) (44, 45), and vesicular stomatitis virus (VSV) (45) also stimulates NLRP3, which then recruits the apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and procaspase-1, forming the NLRP3 inflammasome. How RNA viruses are recognized by NLRP3 is not well-known, but in the case of influenza virus, the proton-selective ion channel M2 protein, not genomic RNA, has been sho...

OBJECT The objective of this study was to describe the surgical anatomy and technical nuances of various vascularized tissue flaps. METHODS The surgical anatomy of various tissue flaps and their vascular pedicles was studied in 5 colored silicone-injected anatomical specimens. Medical records were reviewed of 11 consecutive patients who underwent repair of extensive skull base defects with a combination of various vascularized flaps. RESULTS The supraorbital, supratrochlear, superficial temporal, greater auricular, and occipital arteries contribute to the vascular supply of the pericranium. The pericranial flap can be designed based on an axial blood supply. Laterally, various flaps are supplied by the deep or superficial temporal arteries. The nasoseptal flap is a vascular pedicled flap based on the nasoseptal artery. Patients with extensive skull base defects can undergo effective repair with dual flaps or triple flaps using these pedicled vascularized flaps. CONCLUSIONS Multiple pedicled flaps are available for reconstitution of the skull base. Knowledge of the surgical anatomy of these flaps is crucial for the skull base surgeon. These vascularized tissue flaps can be used effectively as single or combination flaps. Multilayered closure of cranial base defects with vascularized tissue can be used safely and may lead to excellent repair outcomes.

obJect There continues to be confusion over how best to preserve the branches of the facial nerve to the frontalis muscle when elevating a frontotemporal (pterional) scalp flap.The object of this study was to examine the full course of the branches of the facial nerve that must be preserved to maintain innervation of the frontalis muscle during elevation of a frontotemporal scalp flap. methods Dissection was performed to follow the temporal branches of facial nerves along their course in 5 adult, cadaveric heads (n = 10 extracranial facial nerves). results Preserving the nerves to the frontalis muscle requires an understanding of the course of the nerves in 3 areas. The first area is on the outer surface of the temporalis muscle lateral to the superior temporal line (STL) where the interfascial or subfascial approaches are applied, the second is in the area medial to the STL where subpericranial dissection is needed, and the third is along the STL. Preserving the nerves crossing the STL requires an understanding of the complex fascial relationships at this line. It is important to preserve the nerves crossing the lateral and medial parts of the exposure, and the continuity of the nerves as they pass across the STL. Prior descriptions have focused largely on the area superficial to the temporalis muscle lateral to the STL. conclusions Using the interfascial-subpericranial flap and the subfascial-subpericranial flap avoids opening the layer of loose areolar tissue between the temporal fascia and galea in the area lateral to the STL and between the galea and frontal pericranium in the area medial to the STL. It also preserves the continuity of the nerve crossing the STL. This technique allows for the preservation of the nerves to the frontalis muscle along their entire trajectory, from the uppermost part of the parotid gland to the frontalis muscle.